Rapid and non‐genomic reduction of intracellular [Ca2+] induced by aldosterone in human bronchial epithelium

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Abstract
1 Using a Ca2+ imaging system and fura-2 AM (5 μm) we showed that exposure of polarised monolayers of human bronchial epithelial cells (16HBE14o- cell line) to aldosterone produced a fast intracellular [Ca2+] ([Ca2+]i) decrease, in 70 % of cells. Exposure to aldosterone (1 nm) reduced the [Ca2+]i by 39 ± 9 nm (n= 282, P < 0.0001) within 10 min, from a basal [Ca2+]i of 131 ± 19 nm (n= 282). 2 The effect of aldosterone on [Ca2+]i was not affected by inhibitors of the classical genomic pathway, cycloheximide (1 μm) or spironolactone (10 μm). The aldosterone-induced [Ca2+]i decrease was inhibited by thapsigargin (1 μm), pertussis toxin (24 h at 200 ng ml−1), the adenylate cyclase inhibitors 2′,3′-dideoxyadenosine (200 μm) and MDL-12,330A hydrochloride (500 μm), and the protein kinase A inhibitor RP-adenosine 3′,5′-cyclic monophosphorothioate (200 μm). In addition, treatment of 16HBE14o- monolayers with aldosterone (1 nm) inhibited by ≈30 % the large and transient [Ca2+]i increase induced by apical exposure to uridine triphosphate (UTP, 0.1 mm), a known secretagogue in airway epithelia. 3 Our results demonstrate for the first time that in human bronchial epithelial cells, aldosterone decreases [Ca2+]i levels via a non-genomic mechanism. The hormone-induced changes to [Ca2+]i involve stimulation of thapsigargin-sensitive Ca2+-ATPase, via G-protein-, adenylate cyclase- and protein kinase A-coupled signalling pathways.

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